Obesity: Often An Infectious Disease

In the book we attribute obesity mainly to food toxins and malnutrition. Both are well attested as causes of obesity in animals:

  • The easiest way to induce obesity in animals is to feed them a carb toxin and a fat toxin – e.g. wheat, fructose, or alcohol with polyunsaturated fats or hydrogenated trans-fats.
  • Obesity in animals can also be induced by nutrient deficiencies, as in the “methionine-choline deficient diet.”

These causes also seem to be active in humans:

  • Intake of fructose and polyunsaturated fats is strongly associated with obesity in humans.
  • Famine studies show that those who experience a period of severe malnourishment are more likely to become obese.

However, in general we attribute diseases to three causes: food toxins, malnutrition, and infections. This suggests we should look also for infectious causes of obesity.

Adenoviruses Can Cause Obesity in Humans

The study of “infectoobesity,” or pathogen-induced obesity, got underway with the discovery of four viruses that could induce obesity in animals. These four viruses — canine distemper virus, Rous-associated virus type 7, Borna disease virus, scrapie agent – were not able to infect humans. However, in chickens, mice, sheep, goat, dogs, rats and hamsters, these viruses infect the central nervous system and induce obesity through effects on the brain and nerves. [1,2]

But then an avian adenovirus, SMAM-1, was found that infects humans and induces obesity in chickens. SMAM-1 works by a different mechanism; it acts directly on fat cells. [2]

Subsequently 3 human adenoviruses, AD-36, AD-37, and AD-5, have been found that act directly on human fat cells and are associated with human obesity. [2] A group led by Dr. Nikhil Dhurandhar of Wayne State University in Michigan showed that AD-36 can induce obesity when given to chickens, mice, and marmosets. [1]

AD-36 Can Spread By Contact

In Dr. Dhurandhar’s chicken experiments, the virus spread fairly easily. Chickens that shared a cage with an infected bird showed signs of the virus in their blood within 12 hours, suggesting that the virus can be spread by nose or mouth secretions. [3]

To Get Really Fat, You Need an Adenovirus Infection

A new study [4] has given us new information about the prevalence and effects of AD-36 in humans. The study found that 22% of obese children (that is, children in the top 5 percentiles of BMI), but only 7% of non-obese, have AD-36 antibodies. Moreover, among the obese children, those who were AD-36-antibody-positive were much fatter than the other obese children. It seems the top 0.1% of children in BMI are probably overwhelmingly made up of AD-36-infected children.

Metabolic Benefits?

It may not be all bad news. AD-36 promotes proliferation of fat cells. Thus, while it promotes obesity, it may also help prevent diabetes. By creating a bigger pool of fat cells to help clear excess glucose from the blood, toxicity from hyperglycemia is reduced, at least for a time.

In Dr. Dhurandhar’s experiments, the extra fat cells showed metabolic effects consistent with enhanced glucose clearance. Infected chickens had lower serum cholesterol and lower triglyceride levels. [3] So infected chickens are fatter, but in some respects healthier.

Pathogens May Be The Source of Disease Diversity

Close readers of our book may have noticed that a combination of carb and fat toxins is, we believe, the most common cause of metabolic syndrome, diabetes, and obesity.

Yet there are thin diabetics and obese non-diabetics. How is it that the same cause can produce different diseases?

One thing the adenovirus work is telling us is that the nature of one’s chronic infections may determine how bad diets translate into disease. Toxic and malnourishing diets make disease inevitable, but which disease depends on which pathogens happen to be around to exploit the bad diet and weakened immunity.

Lessons for the Non-Obese

I certainly wouldn’t avoid contact with obese people for fear of contracting AD-36. These pathogens are everywhere and infection is inevitable. Most elderly probably have hundreds of chronic infections.

The key to health is not avoiding germs, but maintaining a powerful immune system that prevents pathogens from causing disease. That means a healthy diet, good nutrition, and immune-enhancing practices like fasting and ketogenic diet days.


It appears that:

  • It’s possible to become obese from food toxins and malnutrition alone;
  • Some – it’s not yet clear what fraction – obese people do become obese from food toxins and malnutrition alone;
  • But to become really obese, or to become obese really young, you may need a viral infection to help the obesity along.

In the book, we focus on elimination of food toxins and malnutrition as weight-loss steps. The Perfect Health Diet, controlled to 2,000 calories per day, is a weight loss diet for the obese as well as a healing diet for the metabolic derangements that underly obesity.

What the evidence for adenoviruses in obesity is telling us is that the obese may need to take another dietary step as well:  autophagy-promoting steps like fasting. Autophagy is a primary immune mechanism against viruses, so fasting enhances viral immunity.

As always, we recommend that fasts include substantial amounts of coconut oil to help the liver make ketones and relieve the burden on the liver and the risks of glucose deficiency.


[1] van Ginneken V et al. “Infectobesity”: viral infections (especially with human adenovirus-36: Ad-36) may be a cause of obesity. Med Hypotheses. 2009 Apr;72(4):383-8. http://pmid.us/19138827.

[2] Atkinson RL. Viruses as an etiology of obesity. Mayo Clin Proc. 2007 Oct;82(10):1192-8. http://pmid.us/17908526.

[3] Dhurandhar NV et al. Transmissibility of adenovirus-induced adiposity in a chicken model. Int J Obes Relat Metab Disord. 2001 Jul;25(7):990-6. http://pmid.us/11443497.

[4] Gabbert C et al. Adenovirus 36 and Obesity in Children and Adolescents. Pediatrics. 2010 Sep 20. [Epub ahead of print] http://pmid.us/20855385. See also http://ucsdnews.ucsd.edu/newsrel/health/09-20ViralInfection.asp.

Leave a comment ?


  1. Nice. What is the ETA on the print book?

  2. We’ll deliver the files to the printer this weekend. Should have a proof copy in our hands late next week or early the following week.

    Once we approve the proof copy, we should be able to start delivering copies to buyers of the e-book very quickly. It may take 2 to 6 weeks for the book to become available on Amazon etc.

  3. I´ve had some stomach problems ever since I got sick over a decade ago. First I got a bad cold, sore throat and a fever, soon as I had recovered from that I started to have stomach pain/discomfort and loss of appetite and sometimes nausea. Since then I have had ups and downs, but last year has been particularly bad.

    I´v always wondered if the cold was the trigger for this problem since it came so suddenly. When I mention it I always get vague answers and the doctors have rarely taken it serious, they´ve just blamed it on stress or lack of vegetables(I´ve always liked vegetables).

    The newest diagnos is GERD because of LES, despite never having the burning sensation and I was also told that I was born like this. That made no sense to me so I´m just trying to solve this on my own by changing the diet.

    I see you talk a lot about infections, so I would like your opinion. Could the cold be the trigger for this, that it maybe weakened my immune system to the degree that it opened a pathway to some pathogens that has caused this problem?

  4. Hi Anna,

    Yes, I definitely think the cold may be the original cause of your problems.

    Many chronic infections begin with an acute infection, often very mild, that goes away in a few weeks.

    For an example, you might wish to read the Wheldon’s story, read http://perfecthealthdiet.com/?p=157 and follow the links to the source materials.

    You haven’t really given me enough information to say more. Is the GERD diagnosis based on an endoscopy?

    Best, Paul

  5. Thank you for the response. English is not my language so it´s a bit difficult for me to find the right medical words and I didn´t want to write to much.

    But yes, I had endoscopy few months ago. He said I had loose esophagus spinchter (LES) and prescribed me some PPi (proton pump inhibitor) and told me I had to take it for the rest of my life. I took it for 2 weeks (I wasn´t sure if I was going to take it, but since I was getting bit desperate I decided to try it but I felt even worse).

    I feel better now but I´m still struggling, despite changing my diet. I don´t eat grains, I limit vegetable oils (never use it myself), alcohol and processed food and fructose. I´ve supplemented with vitamin D but I don´t want to take a lot of supplements since I think the stomach doesn´t handle it to well at the moment. I´m still determined to keep on going, and I´m considering your plan and buying the book.

  6. Hi Anna,

    I would basically treat this as a small intestinal infection. I think GERD generally originates in the small intestine, as many GERD cases have bile and pancreatic enzymes in the esophagus and that must mean some kind of small intestinal spasm is shooting the small intestine’s contents up into the esophagus.

    Since your problem started with a cold, there’s good reason to think the problem may be infectious in origin.

    But your pain could be coming from something other than GERD. Is it under the breastbone, or lower? Is it centered or on the right side? Did the endoscopy look at the small intestine? Did they test for H. pylori?

    You’re right to avoid the PPis, they will make infections worse and hurt digestion.

    Check out the bowel disease series, http://perfecthealthdiet.com/?cat=47. I think buying the book and following the general diet would be a good idea, sometimes it’s hard to diagnose a problem but fixing a lot of little things in the diet helps.

    Vitamin D and thyroid/iodine could be important to a solution, I would try to make sure those are optimal.

  7. With the kids going back to school, the flu/cold season will soon be upon us. Do you recommend the same autophagy-activating strategy once we contract the symptoms of such infections?

  8. Hi poisonguy,

    Autophagy activation is great in both prevention and infection-fighting. That may be why most people naturally have minimal appetites during acute infection.

    But in acute infections you should always listen to your body, which knows what it needs. If you get hungry during an infection, eat.

    Best, Paul

  9. Hi Paul,

    only 1/2 thru the ebook, (its great so far), so forgive me if I’ve missed something.

    Can you explain what the role of glucose is in infection fighting. I thought that you’d mentioned that there was a minimum amount needed. If you’re fasting, then aren’t your glucose levels too low to fight infections/yeast with Reactive Oxidative Stress?


  10. Hi DancinPete,

    Yes, that’s right. I don’t recommend fasting if you have a systemic yeast/fungal infection. Beat the fungi first, then start fasting. Also, if you have a systemic fungal infection, eat at the higher end of our glucose range, at least 400 glucose calories per day; supplement iodine in high doses, working up gradually; and take various other anti-fungal steps.

    Best, Paul

  11. Thank you again for your response. I didn´t really expect that someone on the internet would be more interested in this issues than most doctors I´ve talked to.

    I´m actually not sure if they looked at the small intestine, but I think they did though. They also did some kind of biopsy I think, I never heard more about it though so they didn´t tell me of any bacteria. Other than the LES, everything looked fine. The doctor only wanted me to take the medicine. He also made the assumption that because I was lean I had taken care of myself which explained why this “birth defect” didn´t always affect me.

    The pain/discomfort comes exactly from where the stomach is and often comes right after I´ve eaten. I also get the feeling a lot that something is stuck in the esophogus or there is a lot of air that I need to burb which makes it sometimes difficult to breath. If it´s really bad, it can be difficult to stand straight up or do certain excersise like jumping and jogging.

    when it started to get worse again I had been taking Lyrica for chronic headaches (a problem that is even older than this one) for few weeks. When I stopped it the stomach issues got worse for awhile, than got better for few months then last october I got another bad cold and then it got even worse. In January I changed the diet, it was not the magic cure I was hoping for but I think it´s the rigth direction. Now I´m trying to take it even further, giving up nightshades, eggs and dairy and see if that helps.

  12. Hi Anna,

    I take it the Lyrica didn’t help the chronic headaches?

    Headaches are another symptom that often accompanies chronic infection.

    It does sound like GERD. Unfortunately the causes of GERD are not well understood, so I’m a bit at a loss.

    Both my wife and I had GERD and in both cases it went away on our diet, but I couldn’t name any one thing that did the trick. It might be a matter of getting many little things right, and waiting for the body to heal.

    Dr. Eades says some nutritional supplements have done remarkably well at relieving GERD, you might try that. See his post here: http://www.proteinpower.com/drmike/supplements/protexid-and-protexid-nd-and-adventures-in-dr/. The supplements are: melatonin, l-tryptophan,
    vitamin B6, folic acid, vitamin B12, methionine and betaine (trimethylglycine). Choline/lecithin might not be amiss with this combination.

    Good luck!

  13. So it might not be infection after all? Or is it still possible, just one of those things that might have different causes?

    To clarify, I never really disputed the GERD diagnois in itself, just found the explanation and the solution of the doctor inadequate.

    I actually read that many believe GERD is caused by low acid production instead of too much. So I tried taking some Betaine hydrochloric acid for awile. At least I got my appetite for meat again after that (For awhile I was more of vegetarian because I lost my appetite for meat) and that hasn´t changed although I stopped taking it. At least, I found some benefits from more acid, coincident or not.

    Anyway, thank you so much for your interest. I will keep experimenting with diet and read more information. I don´t need doctors for that. But yes, I´m still struggling with headaches and fatigue. I´m hoping diet will also make that better.

    • Hi Anna,

      Well, I think GERD can have multiple causes, one of which is small intestinal infections. But since the endoscopy didn’t show obvious evidence of that, and you haven’t reported intestinal distress, there’s no reason to focus on that possibility.

      The headaches and fatigue are strongly suggestive of chronic infection and high immune activity.

      You and your doctor have to decide whether there are enough indications to justify experimenting with antibiotics, but you should certainly try optimizing immunity through diet, nutrition, and techniques like fasting.

  14. Fascinating stuff!

    Re Viruses: I’ve skimmed through Reference 2 and found it interesting. Specifically, the viral associated/induced obesity was due to a proliferation of adipose tissue and increased triglyceride accumulation in those cells. In most of the human studies cited (but not all), serum cholesterol and triglycerides were LOWER in the antibody + population vs. antibody -. This would indicate to me that this viral induced obesity may actually be “healthy” and not associated with MetS and/or T2 diabetes. Taken together with coincidence of MetS/T2 epidemics and the obesity epidemics, this would seem to indicate that, while they may play a role, viruses are probably not a major contributor. What do you think of that first-glance analysis?

    Re toxins: I wonder if the PUFA=toxin is really a transfat=toxin issue? The whole margarine to replace butter thing didn’t just replace SF’s with PUFA, it introduced transfats. Same for Crisco replacing lard.

    Just found this site (although I may have wandered through before) when I noticed you linked to my blog. I feel honored, THANKS! No doubt I’ll be reading through your work here.

  15. Welcome CarbSane! I’m a fan of your blog and maybe we can get a conversation going from time to time.

    I would agree that it’s healthier to be obese and NOT have met syn / diabetes than to be thin and have diabetes. So, if you’re going to eat a bad diet, maybe it’s a good idea to get some AD-36 to help you tolerate it (for a few decades anyway). But why not eat a good diet and avoid the virus? That should be best of all.

    I think it’s right also that the adenoviruses are not the primary cause of the obesity epidemic, but they do modulate the disease, make weight gain more rapid and weight loss harder. However, we may eventually discover more pathogens that infect the liver and brain and promote obesity. Still early days in “infectobesity” research.

    A general theme of this blog is that disease is the result of the interaction of diet, nutrition, and pathogens. So it may often be the case that for disease to develop you need BOTH a bad diet AND an infection. That could be true of obesity as well. Epidemiologically it looks like increasing fructose/HFCS/soybean oil/canola oil/corn oil consumption was the trigger for the recent obesity epidemic, but that doesn’t exclude pathogen involvement.

    Trans-fats are certainly very toxic but PUFA toxicity is not fully explained by trans-fat content. We have 31 pages in the book going through the literature on PUFA/vegetable oil toxicity. (Since it’s so contentious and complex, this one topic got more space than any other issue.) Sure, hydrogenation makes toxicity worse — though how much of that is because trans-fats are worse than natural omega-6, and how much is due to denaturing of other compounds by the hydrogenation process (we mention hydrogenation of plant vitamin K into dihydrophylloquinone in the book, see http://pmid.us/17684225) is unclear.

    As you read, please let me know my errors! I’d hate to go the way of Gary Taubes. Then again, maybe that wouldn’t be so bad. 🙂

  16. wow, good read…i have a question

    you say a perios of malnutrtion is a cause of obesity. i suffered from anorexia for 6 years, and now have taken steps to get better and restore a good BMI…

    what are my chances of obesity? i do see the corelation between malnourishment and obesity. i dont know that i assimilate all of what i eat or that my gut digestion/flora is where it should be so essentially my body could assume i am ‘lacking’ and put on weight. i dunno if that makes sense

    anyways, do you have any referenes for malnourishment/restricition?

  17. Hi Mallory,

    There are references in the book for malnourishment and obesity, I’ll do a blog post on it sooner or later.

    As for your chances of obesity, I would say that if you eat a healthy diet, they’re close to zero. If you eat the Standard American Diet, your chances are higher than the average American’s. Your children would also have a higher than average chance. Again, a good diet should prevent obesity.

    It’s impossible to make a definite statement for many reasons. One is that only some nutrient deficiencies promote obesity. Deficiency of choline, which is a methyl donor and supports DNA methylation, seems to be a major obesity promoter. Since the effects of malnourishment on obesity are very long-lasting, and can even cross generations, it seems they have to be epigenetic, so a role for methylation makes sense. This suggests that B6/B12/folate deficiencies may also promote obesity.

    I think healing for malnourished people is a long-term process. Eat and supplement optimally, and you’ll probably notice month-to-month improvement for several years at least.

  18. would you please qualify this statement-

    “Famine studies show that those who experience a period of severe malnourishment are more likely to become obese.”

    i have actually heard that the opposite to be true, and have family members who were survivors of the WW2 holocaust (my paternal grandparents) who were healthy after surviving the camps, remained thin throughout life, and lived longer then average lifespans, my grandfather until age 87 when he died of natural causes, peacefully, in his sleep.

    Dr. kurt Harris of paleonu.com mentioned in a post a few months ago, something about people having gone through periods of malnutrition having longer lifespans and this being related to periods of ketosis, though he didnt specify if they were more likely to be obese. im just very curious about the subject. thanks so much.

  19. Hi em,

    There’s ample evidence that calorie restriction extends longevity, as long as there is no nutrient deprivation. So you need adequate quantities of macronutrients (including ~400 calories/day glucose, 200 calories/day protein, 10 calories/day omega-6 and omega-3 fats) plus all the micronutrients, in order for calorie restriction to extend lifespan. But I would not consider this “malnutrition,” just fasting or calorie restriction.

    On the other hand, when nutrients are deprived, there are long-lived health effects. I mentioned above the effect of choline deficiency, which suggests that deficient methylation of DNA chromatin promotes obesity.

    Here’s a reference you might want to look at:

    Stocker CJ et al. Fetal origins of insulin resistance and obesity. Proc Nutr Soc. 2005 May;64(2):143-51. http://pmid.us/15960859.

    It reviews evidence from both humans and animals that nutrient deprivation, e.g. protein deprivation, at very young ages often leads to obesity in later life.

    So it’s really the quality of the diet, rather than the quantity of food, which defines malnutrition.

    Best, Paul

  20. My husband was telling me that in Science an article had pretty much definitively proven the link between chronic fatigue and viruses – of course he could remember the actual virus or the issue of Science – maybe you saw it? There are a number of CFS virus articles in Science over the past couple years.

  21. Paul,

    Perhaps off topic for this post, but what is your advice on determining whether you have good blood sugar control? For example, what are some good numbers to aim for in regard to HbA1C and fasting blood sugar?

  22. Well, it depends a little on how you’re eating. Higher carb intake within our recommended range leads to lower fasting blood glucose for the most part, but possibly higher postprandial blood glucose.

    I would say any HbA1c below 5.5 or so is fine. Below 5 is exceptional. Add coconut oil to lower HbA1c. Eating glucose close to the body’s utilization needs, around 500 calories, will probably minimize HbA1c. I think eating a little less than that is probably optimal for health, but that’s an opinion.

    Fasting blood sugar – you be the judge. Higher means you’re better adapted to do a long fast, lower means you’ll have lower HbA1c which might be good. I would just choose the lifestyle you want / mix of fasting / level of carbs, and be happy with whatever your body comes up with.

  23. Hi Paul,

    You asked CarbSane to let you know about any errors as she reads, so I wanted to mention something from the e-book that may not be an error, but didn’t seem quite on the mark.

    I can’t copy text from the pdf, but at the top of page 18 you state that “methionine excess leads to high homocysteine”, but don’t provide any references to justify the assertion. I had never seen any information to that effect, so after searching recent information it appears that your statement may be in error or at best oversimplifies the actual process, perhaps in the interest of brevity.

    Anyway, I’m not carping or nit-picking, just thought you might welcome the input.

    Here’s one of several references that can be found on the topic at http://tinyurl.com/2833sod


    I’m greatly enjoying the book, btw.

  24. Hi Jim,

    Thanks much, I do welcome pointers to errors.

    Sometime after June that line disappeared from the book. It seems to have been tested and refuted in this paper: http://pmid.us/2261699.

    Sometimes in early drafts we would put in strong statements as markers of items to investigate, and this looks like one of those that didn’t get removed from the June version. There are a few other errors in the June version that have been fixed in the final version.

    If we find any errors in the final version, then I’ll put up an errata page. So please let us know if you notice anything else.

  25. Perfect Health Diet » Perfect Health Diet: Weight Loss Version - pingback on February 1, 2011 at 7:47 pm
  26. http://www.nejm.org/doi/full/10.1056/NEJMsa066082
    “Our study suggests that obesity may spread in social networks in a quantifiable and discernable pattern that depends on the nature of social ties.”

  27. Thanks, eralf! Great point. If obesity spreads through social ties, that would be consistent with an infectious cause.

  28. Though social groups likely share boxes of donuts, too. And they’re not likely to be made of potato starch fried in coconut oil.

  29. Mmmmm … potato starch fried in coconut oil … where can I find that social group?

  30. Dear Paul,
    (and anyone else in the know :-):
    Any studies, theories od suspicions of bacterial pathogens contributing to weight gain? Since struggling with symptoms brought on by eating and that seem bacterial in origin ( early satiety, burping, severe abdominal distention, constipation ) I have also experienced a gradual weight gain that doesn’t seem diectly related to the caloric value of my diet. Worsening symptoms are also accompanied by fluid retention, which also makes me suspicious of an endotoxin. Over the years I’lve experienced a couple of remissions with fairly rapid normalisation of weight, but have rather quickly returned to the above mentioned state. I should be clear that I am not obese, but some 15 lbs above my normal, healthy weight. T3 levels are normalized via medication ( poor conversion of T4 to T3).

    A couple of years ago my daughter, now 11, started gaining weight for nobapparent reason (her diet is very PHD-like). Along with that there’s also a complaint of stomach ache and nausea. Anxiety may account for some of her symptoms, but not all the weight gain (BMI now 21.7). May she have been infected with a pathogen via contact with me?

    For whatever it’s worth, I’ve had several gut infections acquired during travel to tropical regions, and a rather unusual pregnancy with one dead twin remaining in utero together with a healthy one for 4 months ( I’m wondering if the dead baby’s body could have acted as an incubator of sorts since my symptoms started after the pregnancy, gradually worsening over the years) .

    My apologies for the lengthy post, I may have become rather ruthless over the years in my quest to regain my perfect health. I’d also like to take this chance to thank both Paul and other posters for sharing such invaluable information. What a resource this site is!


  31. Hi Lilian,

    It’s definitely the case that gut dysbiosis can promote obesity or, more commonly, 10-20 pounds of weight gain. The mechanism is that immune cells get activated by the gut infection and then these activated immune cells travel to the nearby fat cells and induce them to grab and hold more fat.

    This must be some kind of evolved mechanism to get people to store more resources when their health is threatened.

    I do think infections can often be passed within a family.

    Both you and your daughter might consider getting a stool test like this one: http://www.metametrix.com/test-menu/profiles/gastrointestinal-function/gi-effects-microbial-ecology to see if anything turns up.

    Best, Paul

  32. Paul,
    thanks a million; I’m glad (sort of 🙂 to have my theories confirmed – needless to say our attempts to find help via the medical profession have been futile. We will definitely look into the test, great resource! Looking forward to finally solving his whodunit and focusing our energies on insted enjoying good food, good health and good life!

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